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Table 2 AP properties of hippocampal pyramidal neurons cultured at high density following 48 h pharmacological treatment

From: N-methyl-D-aspartate receptors mediate activity-dependent down-regulation of potassium channel genes during the expression of homeostatic intrinsic plasticity

Treatment

V T (mV)

AP height (mV)

AP rise (ms)

AP decay (ms)

AP HW (ms)

fAHP (mV)

AP latency (ms)

CTL-H2O

−39.4 ± 0.5

64.6 ± 1.3

0.70 ± 0.03

1.72 ± 0.07

1.94 ± 0.07

−19.1 ± 0.6

15.1 ± 0.72

TTX

−40.2 ± 0.7

67.4 ± 1.5

0.67 ± 0.03

1.81 ± 0.08

1.97 ± 0.10

−15.4 ± 0.7**

11.2 ± 0.58**

BC

−37.6 ± 0.4

65.4 ± 2.5

0.60 ± 0.03

1.48 ± 0.14

1.55 ± 0.10

−19.7 ± 1.4#

14.5 ± 0.87

APV

−38.7 ± 1.5

65.6 ± 3.2

0.89 ± 0.05*,##,^^

2.52 ± 0.17**,##,^^

2.56 ± 0.07**,##,^^

−11.5 ± 1.1**,^^

12.9 ± 1.12

TTX + APV

−39.9 ± 0.7

62.8 ± 2.2

0.70 ± 0.02

1.92 ± 0.12$

2.18 ± 0.12^

−15.8 ± 0.9

12.3 ± 0.78

TTX + Nif

−38.4 ± 0.7

63.5 ± 2.3

0.62 ± 0.05$$

1.78 ± 0.13$$

2.04 ± 0.16

−17.6 ± 1.2$$

11.0 ± 0.54*

CTL-DMSO

−39.0 ± 0.9

66.5 ± 1.4

0.76 ± 0.07

1.73 ± 0.19

2.04 ± 0.11

−17.9 ± 1.5

16.1 ± 1.5

Nif

−38.0 ± 0.7

68.2 ± 3.2

0.69 ± 0.05

1.92 ± 0.13

2.07 ± 0.12

−17.5 ± 0.8

16.9 ± 1.0

STO-609

−40.0 ± 0.9

69.3 ± 1.4

0.78 ± 0.05

2.14 ± 0.12

2.26 ± 0.13

−15.9 ± 0.9

16.8 ± 2.0

  1. VT, voltage threshold for action potential; AP, Action potential; rise, 10-90% rise time of AP; decay, 10-90% decay time of AP; HW, half-width; fAHP, fast after-hyperpolarization. AP properties were measured from the first action potential evoked by a current step to 100 pA at a holding potential of −60 mV. Each value represents the mean ± SEM (*p < 0.05, **p < 0.01 for CTL-H2O vs. drug treatment; # p < 0.05, ## p < 0.01 for TTX vs. other drug treatment; ^ p < 0.05, ^^ p < 0.01 for BC vs. other drug treatment; $ p < 0.05, $$ p < 0.01 for APV vs. other drug treatment).